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Bálint Syndrome (including Simultagnosia)
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Visually juggling the many multiples of things competing for our attention is a useful skill, but that skill can diminish or vanish for some people with Bálint syndrome. Sometimes called Bálint-Holmes syndrome, this disorder is characterized by three major symptoms. These symptoms are called a triad because of how often they occur together, although they don't all occur together in every case (Chechlacz & Humphreys, 2014). When combined, these three symptoms have such a severe impact on a person's vision that the person may be mistaken for being blind (Heutink et al., 2019).
Cerebral (cortical) visual impairment in children
Published in John Ravenscroft, The Routledge Handbook of Visual Impairment, 2019
Gordon N. Dutton, Corinna M. Bauer
A 10-year-old boy had had a heart infection when aged 3 (Gillen and Dutton, 2003). This caused indirect damage from bleeding into both posterior parietal lobes. He recovered well, but at age 10 could not read long words, follow text, write words in a line or copy, as print matched to his age had, for him, become too small and crowded. He was losing confidence. He often walked into people as if they were not there, or did not see moving objects like cars and impaired visual scanning was evident. Going down stairs and stepping off kerbs were difficult. Yet his optics, visual acuities, 3D and colour vision were normal. His visual fields could not be plotted because he could not simultaneously see the central and peripheral targets. He could not look at specified targets, but his eye movements to instructions like “look up”, were normal. He took a long time to find an item of clothing in a pile or on a patterned bed spread, or a pencil on a cluttered desk. His behaviours, symptoms, signs and brain imaging were consistent with the diagnosis of a variant of Balint syndrome, comprising inability to see more than one or two items at once at any moment, inaccurate visual guidance of reach and inability to move his eyes to a nominated target. Apparent impairment of his lower visual field, and inability to see fast-moving targets are typical accompaniments.
Clinical presentation and differential diagnosis of dementia in younger people
Published in Marjolein de Vugt, Janet Carter, Understanding Young Onset Dementia, 2021
Yolande A.L. Pijnenburg, Cynthia Klaassen
Posterior Cortical Atrophy (PCA) is the clinico-radiological syndrome that predominantly affects the occipital and parietal lobes, resulting in gradually progressive loss of higher visual functions, apraxia, and elements of the Gerstmann syndrome (Crutch et al., 2013; Crutch et al., 2017). Visual agnosia is a common presentation as well as the Balint syndrome, consisting of oculomotor apraxia, optic ataxia, and simultanagnosia (Moreaud, 2003). Typically, patients experience difficulties in reading, finding or placing objects, finding their way around, and driving. Variants presenting with difficulties in calculation and apraxia have been described. One or multiple visits to an ophthalmologist or optician are a commonly heard story of patients eventually visiting a memory clinic once it is suspected that the problem is not a primary eye issue. Incidentally, their clinical picture has been interpreted as a primary psychiatric disorder. This is particularly the case when the patient displays a Balint syndrome, as these patients cannot generate a visual overview of a space filled with objects and/or persons, whereas, on the other hand, they can identify details that catch their eyes. At onset, patients with PCA are mostly aware of their deficits, and when isolated disturbances in the visuospatial domain are present, they can remain independent in instrumental daily living activities. However, when the syndrome progresses, language and memory difficulties will emerge. These patients may benefit from support by occupational therapists or healthcare workers specialised in low vision. Although Alzheimer's disease is the most common underlying pathology, PCA is mostly considered a variant of Alzheimer's disease. Underlying corticobasal degeneration or Lewy body disease have also been described (Crutch et al., 2012).
Numeric input operation on electronic devices among individuals with visuospatial working memory impairment
Published in Neuropsychological Rehabilitation, 2021
Kosaku Sunagawa, Michitaka Funayama, Yoshitaka Nakagawa, Rumi Tanemura
Regarding visuospatial function, individuals with Bálint syndrome (Bálint, 1909) or unilateral spatial neglect (USN) bear all the characteristics of visuospatial deficits. The characteristic Bálint syndrome is categorized into three signs: psychic paralysis of gaze, spatial disorder of attention, and optic ataxia. Psychic paralysis of gaze is the inability to voluntarily shift one’s gaze to objects of interest despite unrestricted ocular movement. Spatial disorder of attention is also known as dorsal simultaneous agnosia (Luria, 1959; Rizzo & Vecera, 2002) and results in the in ability to perceive several items in a visual scene at any one time. Optic ataxia refers to a difficulty in reaching under visual guidance that occurs in the absence of any muscle weakness. In daily life, patients with Bálint syndrome have difficulties finding objects and remembering locations as well as spatial relationships between objects. Patients with USN often appear to be unaware of contralesional stimuli, a deficit that cannot be accounted for by deafferentation. It is thought that many symptoms of neglect are related to attention deficits (Heilman, Watson, & Valenstein, 1993). Left USN after a right hemispheric lesion is also more long-lasting and chronically affects activities of daily living (Spaccavento, Cellamare, Falcone, Loverre, & Nardulli, 2017; Ten Brink, Verwer, Biesbroek, Visser-Meily, & Nijboer, 2017).
Posterior cortical atrophy: clinical, neuroimaging, and neuropathological features
Published in Expert Review of Neurotherapeutics, 2023
John Best, Marianne Chapleau, Gil D. Rabinovici
Following Benson’s initial report, additional case series were published highlighting the clinical and radiographic features of PCA. Presenting symptoms classically include a variety of deficits in higher-order visual processing but can also include a number of nonvisual deficits which localize toposterior parietal regions. The most frequent visual symptoms are spatial perception deficits (i.e. where objects are in space) as well as object perception deficits (i.e. visual agnosia). Patients develop features of Gerstmann Syndrome, including agraphia (inability to write), acalculia (impaired mental calculations), finger agnosia (loss of ability to name and distinguish fingers), and right-left dissociation. Features of Balint syndrome, including oculomotor apraxia (impaired voluntary and purposeful eye movements), optic ataxia (inability to accurately reach toward an object under visual guidance), and simultanagnosia (the inability to simultaneously process and integrate multiple visual inputs), are also commonly present. Visual field defects are often detected, especially when formally assessed with perimetry. Function in other cognitive domains is generally preserved until more advanced stages of the disease, although visual memory can be impacted early in the disease course [2]. The syndrome’s name is derived from the profound atrophy, hypometabolism and hypoperfusion of parieto-occipital and parieto-temporal visual association cortices noted on structural and functional brain imaging [1,3]. Neuropathologic series of patients diagnosed with PCA during life and followed to autopsy have found that the PCA clinical syndrome is most frequently associated with Alzheimer’s disease (AD) neuropathologic changes and is therefore sometimes referred to as the ‘visual variant of AD’ The most common alternative pathologies are Lewy Body Disease and corticobasal degeneration [4,5]. Prion disease has been described with an initial PCA presentation but is exceedingly rare [4].